Thapsigargin (TG) is a naturally-occurring compound that is highly specific for inhibiting the sarco/endoplasmic reticulum and endoplasmic reticulum Ca2+-ATPase pump (SERCA). The inventors recently identified TG as a modulator of Notch (Roti G., et al., “Complementary genomic screens identify SERCA as a therapeutic target in NOTCH1 mutated cancer.” Cancer Cell, 2013, 23(3):390-405.). The inhibition of SERCA leads to Notch inactivation, which inhibits T-cell acute lymphoblastic leukemia (T-ALL) growth both in vitro and in vivo. However, inhibition of the SERCA pump induced by TG leads to an initial depletion of the endoplasmic reticulum (ER) Ca2+ pool, which ultimately results in on increase in intracellular calcium. Therefore, prolonged exposure to TG could induce apoptosis in a variety of rapidly proliferating cell types in vitro. Thapsigargin is able to kill proliferatively quiescent G0 cells, but is non-specific for any cell types. Therefore, it is difficult to administer and deliver TG systemically due to significant nonspecific host toxicity (e.g., cardiac toxicity). Therefore, there remains a need to develop methods for selectivity delivering to rapidly proliferating cells a composition having the toxicity and activity of thapsigargin.